Cigarette smoke extract-induced interleukin-6 expression is regulated by phospholipase D1 in human bronchial epithelial cells

Koo, Jun Bon; Han, Joong‐Soo

doi:10.2131/jts.41.77

Cited by 21 publications

(9 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[30] These inflammatory mediators are secreted from epithelial cells and may further act on other immune cell types, such as mast or T cells, triggering an inflammatory cascade. The findings of our study are consistent with those of Koo et al [31] Furthermore, CSC is found to promote the expression and release of the proinflammatory cytokine nerve growth factor in bronchial epithelial cells. [32] We also demonstrated that CSC upregulated the expression of EC-SOD, MDA, and 8-OHdG while downregulating the expression of GSH.…”

Section: Discussionsupporting

confidence: 93%

Identification of apoptosis‐associated protein factors distinctly expressed in cigarette smoke condensate‐exposed airway bronchial epithelial cells

Lin¹,

Tian³

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Smoking is associated with an increased risk of respiratory diseases, including lung cancer and asthma. However, the mechanisms or diagnostic markers for smoking‐related diseases remain largely unknown. Here we investigated the role of cigarette smoke condensate (CSC) in the regulation of human bronchial epithelial cell (BEAS‐2B) behavior. We found that exposure to CSC significantly inhibited BEAS‐2B cell viability, impaired cell morphology, induced cell apoptosis, triggered oxidative damage, and promoted inflammatory response, which suggests a deleterious effect of CSC on bronchial epithelial cells. In addition, CSC markedly altered the expression of apoptosis‐associated protein factors, including p21, soluble tumor necrosis factor receptor 1, and Fas ligand. In sum, our study identified a panel of novel protein factors that may mediate the actions of CSC on bronchial epithelial cells and have a predictive value for the development and progression of smoking‐related diseases, thus providing insights into the development of potential diagnostic and therapeutic strategies against these diseases.

show abstract

Section: Discussionsupporting

confidence: 93%

Identification of apoptosis‐associated protein factors distinctly expressed in cigarette smoke condensate‐exposed airway bronchial epithelial cells

Lin¹,

Tian³

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

show abstract

“…PM2.5 adsorbed more harmful substances including metals and polycyclic aromatic hydrocarbons, which can be delivered easily through the respiratory tract inducing the damage of airway epithelial cell 32 33 . Thus, compound 2 may have the potential to be developed as a lead drug to relieve the injury of airway epithelial cell caused by external environment or cigarette smoke 34 . By contrast, due to the low production level of compound 3 and other xylosides (compounds 6 to 11 ), their biological activities did not evaluate further.…”

Section: Discussionmentioning

confidence: 99%

Discovery of novel xylosides in co-culture of basidiomycetes Trametes versicolor and Ganoderma applanatum by integrated metabolomics and bioinformatics

Yao

Zhu

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Transcriptomic analysis of cultured fungi suggests that many genes for secondary metabolite synthesis are presumably silent under standard laboratory condition. In order to investigate the expression of silent genes in symbiotic systems, 136 fungi-fungi symbiotic systems were built up by co-culturing seventeen basidiomycetes, among which the co-culture of Trametes versicolor and Ganoderma applanatum demonstrated the strongest coloration of confrontation zones. Metabolomics study of this co-culture discovered that sixty-two features were either newly synthesized or highly produced in the co-culture compared with individual cultures. Molecular network analysis highlighted a subnetwork including two novel xylosides (compounds 2 and 3). Compound 2 was further identified as N-(4-methoxyphenyl)formamide 2-O-β-D-xyloside and was revealed to have the potential to enhance the cell viability of human immortalized bronchial epithelial cell line of Beas-2B. Moreover, bioinformatics and transcriptional analysis of T. versicolor revealed a potential candidate gene (GI: 636605689) encoding xylosyltransferases for xylosylation. Additionally, 3-phenyllactic acid and orsellinic acid were detected for the first time in G. applanatum, which may be ascribed to response against T.versicolor stress. In general, the described co-culture platform provides a powerful tool to discover novel metabolites and help gain insights into the mechanism of silent gene activation in fungal defense.

show abstract

“…IL-17 induces tissue inflammation mainly by stimulating the expression of several proinflammatory cytokines including IL-6, TNF-α, IL-1β, and IL-8 [20]. This leads to the expansion and accumulation of neutrophils in the focus of inflammation, as occurs, for example, in smoke-induced injury [21][22][23]. The formation of a Th17 cell subset is initiated by transforming growth factor-(TGF-) β together with the obligatory presence of IL-6 [24].…”

Section: Introductionmentioning

confidence: 99%

High Serum Level of IL-17 in Patients with Chronic Obstructive Pulmonary Disease and the Alpha-1 Antitrypsin PiZ Allele

et al. 2020

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is multifactorial disease, which is characterized by airflow limitation and can be provoked by genetic factors, including carriage of the PiZ allele of the protease inhibitor (Pi) gene, encoding alpha-1 antitrypsin (A1AT). Both homozygous and heterozygous PiZ allele carriers can develop COPD. It was found recently that normal A1AT regulates cytokine levels, including IL-17, which is involved in COPD progression. The aim of this study was to determine whether homozygous or heterozygous PiZ allele carriage leads to elevated level of IL-17 and other proinflammatory cytokines in COPD patients. Materials and Methods. Serum samples and clinical data were obtained from 44 COPD patients, who included 6 PiZZ, 8 PiMZ, and 30 PiMM A1AT phenotype carriers. Serum concentrations of IL-17, IL-6, IL-8, IFN-γ, and TNF-α were measured by the enzyme-linked immunosorbent assay (ELISA). All A1AT phenotypes were verified by narrow pH range isoelectrofocusing with selective A1AT staining. A turbidimetric method was used for quantitative A1AT measurements. Results. COPD patients with both PiZZ and PiMZ phenotypes demonstrated elevated IL-17 and decreased IFN-γ levels in comparison to patients with the PiMM phenotype of A1AT. Thereafter, the ratio IL-17/IFN-γ in PiZZ and PiMZ groups greatly exceeded the values of the PiMM group. Homozygous PiZ allele carriers also had significantly higher levels of IL-6 and lower levels of IL-8, and IL-6 values correlated negatively with A1AT concentrations. Conclusions. The presence of the PiZ allele in both homozygous and heterozygous states is associated with altered serum cytokine levels, including elevated IL-17, IL-17/IFN-γ ratio, and IL-6 (only PiZZ), but lower IFN-γ and IL-8.

show abstract

Cigarette smoke extract-induced interleukin-6 expression is regulated by phospholipase D1 in human bronchial epithelial cells

Cited by 21 publications

References 66 publications

Identification of apoptosis‐associated protein factors distinctly expressed in cigarette smoke condensate‐exposed airway bronchial epithelial cells

Identification of apoptosis‐associated protein factors distinctly expressed in cigarette smoke condensate‐exposed airway bronchial epithelial cells

Discovery of novel xylosides in co-culture of basidiomycetes Trametes versicolor and Ganoderma applanatum by integrated metabolomics and bioinformatics

High Serum Level of IL-17 in Patients with Chronic Obstructive Pulmonary Disease and the Alpha-1 Antitrypsin PiZ Allele

Contact Info

Product

Resources

About